Daddy Issues: Paternal Effects on Phenotype

Rando, Oliver J.

doi:10.1016/j.cell.2012.10.020

Cited by 261 publications

(237 citation statements)

References 49 publications

(65 reference statements)

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“…62 While fathers cannot provide direct nourishment to the young after birth, additional attention should be paid to whether a healthy diet of the father, and the mother, before conception can lead to long-term beneficial offspring consequences. It is increasingly becoming apparent that sub-optimal paternal diets, those high in fat or protein restricted, can result in negative offspring sequelae, [14][15][16][17][18][19][20][21][146][147][148][149] but the impacts of a healthy diet have been largely ignored. In conclusion, much work remains on identifying various steps that both parents can adapt to ensure the lifelong health of their offspring and potentially even triumph over negative influences that the conceptus or neonate may encounter.…”

Section: Discussionmentioning

confidence: 99%

“…4,[6][7][8][9][10][11][12][13] It is also increasingly becoming apparent that the environmental state of both the mother and father can underpin later diseases in offspring, even those who appear healthy at birth. [14][15][16][17][18][19][20][21][22][23][24][25][26] Such intrinsic and extrinsic factors in animal models and humans include exposure to endocrine disrupting chemicals, such as bisphenol A, phthalates, heavy metals, stress, obesity, high fat/ high caloric diets, metabolic status and starvation conditions to provide a few examples. It is also clear that in general, males may be at greater risk for later disorders, including those of the cardiovascular and neurological systems, than females.…”

Section: Introductionmentioning

confidence: 99%

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Homage to the ‘H’ in developmental origins of health and disease

Rosenfeld

2016

J Dev Orig Health Dis

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Abundant evidence exists linking maternal and paternal environments from pericopconception through the postnatal period to later risk to offspring diseases. This concept was first articulated by the late Sir David Barker and as such coined the Barker Hypothesis. The term was then mutated to Fetal Origins of Adult Disease and finally broadened to developmental origins of adult health and disease (DOHaD) in recognition that the perinatal environment can shape both health and disease in resulting offspring. Developmental exposure to various factors, including stress, obesity, caloric-rich diets and environmental chemicals can lead to detrimental offspring health outcomes. However, less attention has been paid to date on measures that parents can take to promote the long-term health of their offspring. In essence, have we neglected to consider the ‘H’ in DOHaD? It is the ‘H’ component that should be of primary concern to expecting mothers and fathers and those seeking to have children. While it may not be possible to eliminate exposure to all pernicious factors, prevention/remediation strategies may tip the scale to health rather than disease. By understanding disruptive DOHaD mechanisms, it may also illuminate behavioral modifications that parents can adapt before fertilization and throughout the neonatal period to promote the lifelong health of their male and female offspring. Three possibilities will be explored in the current review: parental exercise, probiotic supplementation and breastfeeding in the case of mothers. The ‘H’ paradigm should be the focus going forward as a healthy start can indeed last a lifetime.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Homage to the ‘H’ in developmental origins of health and disease

Rosenfeld

2016

J Dev Orig Health Dis

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“…We have now learned, a mutation in a single gene can cause multiple distinct entities, a single phenotype can be caused by mutations in one of a number of genes, and variations in the phenotype caused by a mutation in a single gene are larger than expected [Hennekam, 2007]. Indeed, disorders that can be completely explained by a mutation in a single gene ("truly monogenic disorders") do not seem to exist [Hennekam and Biesecker, 2012]; the effect of the primary locus is substantially influenced by sequence variants elsewhere in the genome [Slavotinek and Biesecker, 2003], epigenetic phenomena such as imprinting [Rando, 2012], topologic attributes of chromosomes [Cremer et al, 2006], and so on. Therefore, it is no longer appropriate to require "a single cause" for the definition of a syndrome.…”

Section: Discussionmentioning

confidence: 99%

Elements of morphology: General terms for congenital anomalies

Hennekam

Biesecker

Allanson

et al. 2013

American J of Med Genetics Pt A

124

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An international group of clinicians working in the field of dysmorphology has established a process for the standardization of terms used to describe human morphology. The goals are to standardize these terms and develop consensus regarding their definitions. This project will increase the usefulness and precision of descriptions of the human phenotype and facilitate reliable comparisons of phenotypic findings among clinicians and researchers in medicine, developmental biology, and genetics. Here we define and illustrate the general terms that describe congenital anomalies as related to human conditions.

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“…Accordingly, in these models, the sires can be removed from the cage upon pregnancy of the dam. Thus, paternal metabolism and behaviour do not contribute to the offspring's phenotype and the inheritance of nutritionally acquired phenotypes can be attributed, in part, to epigenetic mechanisms (40,41) . However, it has to be noted that additional carriers might contribute to such paternal effects, including paternal transfer of the microbiota or elements contained in the seminal fluid (42) .…”

Section: Maternal V Paternal Effectsmentioning

confidence: 99%

Transgenerational epigenetic inheritance of diabetes risk as a consequence of early nutritional imbalances

et al. 2015

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Conference on 'Diet, gene regulation and metabolic disease' Symposium 3: Nutrition, epigenetics and the fetal origins of metabolic disease In today's world, there is an unprecedented rise in the prevalence of chronic metabolic diseases, including obesity, insulin resistance and type 2 diabetes (T2D). The pathogenesis of T2D includes both genetic and environmental factors, such as excessive energy intake and physical inactivity. It has recently been suggested that environmental factors experienced during early stages of development, including the intrauterine and neonatal periods, might play a major role in predisposing individuals to T2D. Furthermore, several studies have shown that such early environmental conditions might even contribute to disease risk in further generations. In this review, we summarise recent data describing how parental nutrition during development increases the risk of diabetes in the offspring. We also discuss the potential mechanisms underlying transgenerational inheritance of metabolic disease, with particular emphasis on epigenetic mechanisms.

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Daddy Issues: Paternal Effects on Phenotype

Cited by 261 publications

References 49 publications

Homage to the ‘H’ in developmental origins of health and disease

Homage to the ‘H’ in developmental origins of health and disease

Elements of morphology: General terms for congenital anomalies

Transgenerational epigenetic inheritance of diabetes risk as a consequence of early nutritional imbalances

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